4/8/08. Brad Weaver Schistosome Parasitic blood fluke of trematode family Prevalent in tropics – 200 million people affected Acute infection - swimmer’s.

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Presentation transcript:

4/8/08

Brad Weaver

Schistosome Parasitic blood fluke of trematode family Prevalent in tropics – 200 million people affected Acute infection - swimmer’s itch and Katayama fever Chronic infection – deposited eggs invade tissue and get lodged in portal circulation causing inflammation and fibrosis Two types of renal disease Urinary obstruction from S. haematobium Immune complex deposition disease from other species

S. haematobium Direct invasion of urinary system Acquired in North Africa, Turkey, the Middle East, and India Eggs migrate from vesical venous plexus into bladder wall and then are excreted in urine Often presents with hematuria Chronic inflammation and fibrosis of bladder wall can cause: Hydronephrosis and calcification of urinary tract Bladder cancer

S. mansoni and S. japonicum Acquired in tropical areas of Africa, Asia, South America, and the Caribbean Eggs released from mesenteric venous plexus can travel to intestine OR enter portal blood flow and get lodged in liver sinusoids Eggs in liver sinusoids can cause: Inflammation and progressive fibrosis Secondary portal hypertension and liver failure

Glomerular disease Immune complex deposition Affects 10-15% with chronic infection Two observations Antibodies to schistosomal antigens can be detected in glomeruli Schistosomal antigens can be detected in glomeruli by indirect immunofluorescense Wide variety of clinical manifestations Proteinuria Nephrotic syndrome ESRD Sobh et al. Kidney Int 1987; 31:1006.

The “liver effect” Interplay between portal hypertension/portosystemic shunting and glomerular disease Kupffer cells of the liver remove circulating immune complexes and Schistosome antigens As liver disease worsens in chronic Schistosome infections, there is increased delivery of immune complexes and antigens to glomeruli

Pathology - AFRAN classification Class I – mesangial proliferative glomerulonephritis Class II – exudative glomerulonephritis, many neutrophils and monocytes, associated with dual salmonella infection Class III – MPGN, more common in non-blacks Class IV – FSGS, more common in blacks Class V - amyloidosis

Pathology cont. AFRAN classes I and II have good prognosis and do not progress AFRAN classes III and IV are progressive diseases, often lead to ESRD, and are not modified by antihelminthic drugs or immunosuppressive agents (prednisone and cyclophosphamide)

Diagnosis and treatment Peripheral eosinophilia present in up to 2/3 of those infected Egg detection by microscopy Most common method of diagnosis of Schistosomal infection Stool O&P for all species except S. haematobium (urine micro) Maximal egg excretion occurs between 10am and 2pm Other tests available, lack standardization: ELISA, PCR Treatment: praziquantel (Biltricide) 600mg tid x 1 day